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Jaundice in Children

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Jaundice in Children Abdulwahab Telmesani FRCPC,FFAP Faculty of Medicine and Medical Science Umm Al-Qura University An Approach to a Child With Direct ... – PowerPoint PPT presentation

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Title: Jaundice in Children


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Jaundice in Children
  • Abdulwahab Telmesani
  • FRCPC,FFAP
  • Faculty of Medicine and Medical Science
  • Umm Al-Qura University

3
An Approach to a Child With Direct
Hyperbilirubinemia
4
Classic Approach
  • Proper detailed history
  • Proper physical examination
  • Formalize an impression of prioritized DDx
  • Appropriate investigations

5
Identify
  • Acute
  • Chronic (more than 6 months)

6
In Children
  • Acute
  • Chronic (more than 6 months)

7
Identify
  • Hepatocellular
  • Chlestatic

8
In Children
  • Hepatocellular (ALT/AST more than twice of ALP)
  • Cholestatic (ALT/AST less than twice of ALP)

9
Remember
  • The prognostic value of
  • Albumin
  • Coagulation profile

10
Etiology
  • Infection
  • Drugs
  • Specific Entities
  • Vascular

11
Etiology
  • Infection
  • Drugs
  • Specific Entities
  • Vascular

12
Infections
  • Viral
  • Bacterial
  • Parasitic

13
Viral Hepatitis
  • Hepatotropic Viruss
  • (replicate in the liver and causes
    hepatitis)
  • Others

14
Hepatotropic Viruses
  • HBV (10-20 Chronic active hepatitis)
  • HCV (70-80 Chronic active hepatitis)

15
Hepatotropic Viruses
  • Non B / C Viral Hepatitis
  • HAV
  • HEV
  • HFV
  • HGV
  • TTV
  • SEN

16
Others
  • EBV
  • CMV
  • Herpes
  • Other

17
Hepatitis A Virus
  • Most common cause of community acquired hepatitis
    through out the world

18
Hepatitis A Virus
  • RNA Picorna Virus (Rhinovirus, Enterovirus,
    Cocxackievirus)
  • Feco - oral transmission (Food borne /- Water
    borne)
  • Day care centers account for 10 of cases

19
Hepatitis A Virus
  • Transmission in 50 of contacts

20
Hepatitis A Virus
  • Liver injury in HAV is secondary to immune
    response not to cytopathy

21
Hepatitis A Virus
  • Presentation
  • Incubation period 4 weeks
  • Prodrome 1 week
  • Jaundice 1 3 weeks
  • Hepatomegaly
  • Liver enzymes 20 100 time upper normal
  • Spontaneous resolution

22
Hepatitis A Virus
  • Presentation
  • Sporadic
  • Epidemic
  • Endemic

23
Geographic Distribution of HAV Infection
24
Hepatitis A Virus
  • Clinical Presentation in Endemic areas
  • 10 of children below 6 years
  • 40 of children 6 14 years
  • 70 of subjects older than 14 years
  • 70 100 of children have been infected

25
Hepatitis A Virus
  • Epidemic
  • Tend to seasonal
  • Symptoms as in sporadic cases

26
Hepatitis A Virus
  • No Chronic Sequelae

27
Hepatitis A Virus
  • Variants
  • Relapsing course up to 1 year
  • Cholestatic up to 2 years
  • Immune-complex features ( vasculitis,
    arthritis)

28
Hepatitis A Virus
  • Fatalities
  • Secondary to acute hepatic failure
  • Less than 2
  • More in older children and adults
  • When on top of chronic hepatitis

29
Hepatitis A Virus
  • In Shanghais HVA epidemic, mortality was 5 times
    higher among patients with chronic hepatitis B

30
Hepatitis A Virus
  • Prevention
  • Immunoglobulin
  • Vaccination
  • ( 2 doses 6 months apart above 1 year of age)

31
Hepatitis A Virus
  • ? Atopy protect against enteric infection
  • including HAV
  • P
    N Black Allergy 2005

32
Hepatitis B Virus
  • Vaccination decreased the incidence of hepatic
  • carcinoma in children (in adults in future)

33
Hepatitis C Virus
  • Perinatal transmission about 6
  • Elective C/S might lower the risk
  • No evidence of risk of breast feeding

34
Hepatitis E Virus
  • Single Strand RNA
  • Feco oral transmission
  • Endemic in Tropical and Subtropical countries
  • Mortalities 0.2 but as high as 4 in pregnant
    women

35
Hepatitis E Virus
  • Incubation period 2 9 weeks
  • Presentation similar to Hepatitis A
  • Diagnosed by Anti HEV IGM serology
  • No chronic sequelae reported
  • It worsens chronic hepatitis
  • No vaccine available yet

36
Hepatitis G Virus
  • Enveloped RNA virus
  • Parental transmission
  • Detected by PCR
  • 2-39 of non A-E hepatitis
  • 16-43 of Fulminant hepatitis
  • ? Hepatotropic
  • No established serology

37
TTV
  • Single strand DNA
  • Isolated from patients post transfusion (100 )
  • Isolated from patients with non A-E Hepatitis
  • Presents in health individuals 1 13 (89 )
  • ? Feco oral transmission
  • ? Normal human viral flora

38
SEN Virus
  • Single strand DNA virus
  • Most recent cause of non A- E Hepatitis
  • Found in Blood donors 1- 13
  • In 70 of transfused patients
  • ? Hepatotropic
  • ? Feco oral transmission.

39
Etiology
  • Infection
  • Drugs
  • Specific Entities
  • Vascular

40
Paracetamol
  • Commonest cause of acute liver failure in USA
  • We all have it at home
  • Toxic dose is more than 150 mg /Kg

41
Paracetamol
  • Need repeated serum drug level
  • Follow Rumack-Matthew nomogram
  • A point of irreversible liver damage (end stage
    liver disease)
  • N-cetylcysteine is the anti-dote
    (oral/intravenous)
  • Liver transplant when end stage liver disease

42
Etiology
  • Infection
  • Drugs
  • Specific Entities
  • Vascular

43
Specific Entities
  • Wilsons Disease
  • A1 Antitrypsin deficiency
  • IBD Hepatitis
  • Auto-immune Hepatitis
  • Syndromatic Diseases
  • Metabolic
  • Progressive Familial Intrahepatic Cholestasis

44
Wilsons Disease
  • Autosomal Recessive Disease
  • Low cerulplasmin
  • Copper deposition in
  • liver,
  • brain,
  • kidneys,
  • eyes,
  • heart,
  • Hemolysis

45
Wilsons Disease
  • Presents in any of the following
  • Acute liver disease
  • Chronic liver disease
  • Minimal neurological manifestations
  • Sever neurological manifestations
  • Psychiatric symptoms
  • Renal tubular acidosis
  • Bony deformities
  • Hemolytic anemia

46
Wilsons Disease
  • An 18 years old male and 19 years female
    reported with Schizophrenic symptoms
  • No Kayser -Fleischer ring
  • Normal physical examination
  • Low cerulplasmin, high serum copper and high 24
    HR urine copper
  • Symptoms improved on D Penicillamine

  • Patrick Stiller J Psych. Neurosci 2002

47
Wilsons Disease
  • Liver biopsy and determination of hepatic copper
    is the golden standard for diagnosis of Wilsons
    Disease

48
Wilsons Disease
  • Diagnosis can be made based on at least two
  • of the following
  • Low serum Cerulplasmin
  • High 24 HR urine copper
  • K.F Ring

  • Ashish Bavdekar

  • J
    Gastr Hepat 2004

49
Wilsons Disease
  • Treatment
  • D- Penicillamine
  • Trientine
  • Zinc

50
Etiology
  • Infection
  • Drugs
  • Specific Entities
  • Vascular

51
Vascular
  • Sickle cell Disease
  • Budd - Chiari Syndrome
  • Constrictive Pericarditis
  • Veno - occlusive disease seen with chemotherapy

52
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